Docosahexaenoic acid prevented tumor necrosis factor alpha-induced endothelial dysfunction and senescence

被引：30
|
作者：
Yamagata, Kazuo [1 ]
Suzuki, Sayaka [1 ]
Tagami, Motoki [2 ]
机构：
[1] Nihon Univ NUBS, Coll Bioresource Sci, Dept Food Biosci & Biotechnol, Fujisawa, Kanagawa, Japan
[2] Sanraku Hosp, Dept Internal Med, Chiyoda Ku, Tokyo, Japan
来源：
PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS | 2016年 / 104卷
关键词：
Endothelial cells; Dysfunction; Senescence; DHA; TNF alpha; DENSITY-LIPOPROTEIN RECEPTOR-1; TNF-ALPHA; OXIDATIVE STRESS; CELL-ADHESION; GROWTH-FACTOR; LIFE-SPAN; EXPRESSION; P66(SHC); GENE; PHENOTYPE;
D O I：
10.1016/j.plefa.2015.10.006
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
We investigated how docosahexaenoic acid (DHA) regulated tumor necrosis factor-alpha (TNF-alpha)-induced senescence and dysfunction in endothelial cells (EC). We used RT-PCR to examine the expression of several genes related to senescence and dysfunction in EC. TNF-alpha-induced p21 protein levels were investigated by Western blot (WB) and fluorescence antibody techniques. TNF-alpha induced the senescence marker P-galactosidase and the expression of several senescence and endothelial dysfunction-related genes, e.g., CDKN1A, SHC1 and GLB1. DHA attenuated TNF-alpha-induced senescence-related gene expression and p21 protein expression. DHA attenuated TNF-alpha-induced gene expression related to dysfunction of EC, such as plasminogen activator inhibitor 1 (SERPINE1), lectin-like oxidized low-density lipoprotein receptor-1 (OLR1), thromboxane A2 receptor (TXA2R) and p38 MAPK (MAPK14). DHA reversed the TNF-alpha-mediated reduction of endothelial nitric oxide synthase (NOS3) gene expression. TNF-alpha-mediated upregulation of these genes was inhibited by allopurinol and apocynin. These results indicated that DHA regulated the expression of several genes that are associated with senescence and dysfunction of EC. (C) 2015 Elsevier Ltd. All rights reserved.
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收藏
页码：11 / 18
页数：8
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